Tuesday, 13 January 2015

COPD

There are 30,000 deaths per year attributable to COPD.

Pathogenesis of COPD
 COPD is an umbrella term for any airflow obstruction respiratory term. It includes emphysema, chronic bronchitis, resistent asthma, bronchiectasis and to a certain extent, cystic fibrosis.
Most of it is caused by damage to the lungs from smoking. Cases in young people (younger than 45) should raise the possibility of alpha - 1 - antitrypsin deficiency (2%). Alpha-1-antitypsin protects the alveoli, and deficiency is congenital co-dominant.
Occupational triggers are also possible - heavy exposure to occupational dusts and chemicals, air pollution and cannabis smoking is now being recognised as a cause.



18% of all smokers aged over 35 years will have airflow obstruction
27% of all smokers aged over 35 years with chronic cough will have airflow obstruction
48% of all smokers aged over 60 years and chronic cough will have airflow obstruction

Clinical Presentation
.
Considered in patients > 35 who have a risk factor and one or more of:
exertional breathlessness
chronic cough
regular sputum production
frequent winter "bronchitis"
wheeze


Signs of right heart failure such as raised JVP, peripheral oedema, hepatomegaly




Rule out red flags for other disease before diagnosing COPD (weight loss, effort intolerance, waking at night, ankle swelling, fatigue, occupational hazards, chest pain, haemoptysis)







Investigations
Spirometry:
Airflow obstruction: reduced FEV1/FVC ratio: FEV1/FVC is less than 0.7.
Fixed 70% ratio may mean that COPD is being over-diagnosed in elderly people and under-diagnosed in young people.




Chest X-ray
- Increased bronchovascular markings
- Cardiomegaly
- Lung hyperinflation with flattened hemidiaphragms
- Possible bullous changes.

A full blood count to identify anaemia or polycythaemia
An assessment of body mass index (BMI).


It's difficult to completely differentiate COPD from asthma. NICE guidelines have some recommendations.




Treatment Options
Primary prevention (stopping smoking) is the most important intervention. The next step is to ensure a timely diagnosis. Beta blockers are safe.
Inhalers in COPD are used to prevent and control symptoms, reduce the frequency and severity of exacerbations, improve health status and improve exercise tolerance. Stopping smoking is the only measure that can prevent deterioration.

Tiotropium HandiHaler - long-acting antimuscarinic bronchodilator (LAMA). It is once-daily dosing and the most common side effect is dry mouth.

Seretide - a very expensive inhaler. 


Mucolytics - Increase expectoration of sputum by reducing its viscosity. They can reduce the number of exacerbations and improve symptoms of cough production:
Carbocisteine 750 mg three times daily, reducing to 1.5 g daily in divided doses
Mecysteine 200 mg three times daily for 6 weeks reducing to 200 mg twice daily

LTOT - PaO2 less than 7.3 kPa when stable or a PaO2 greater than 7.3 and less than 8 kPa when stable and one of:
secondary polycythaemia
nocturnal hypoxaemia
peripheral oedema
pulmonary hypertension

End of Life Care
Patients can die quickly after a COPD exacerbation. It is important that their plans for care at the end of life are discussed and documented. Opioids should be used to alleviate breathlessness at the end of life. Benzodiazepines can be considered.

References
See next blog post
Pictures from http://calgaryguide.ucalgary.ca/ 


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